口服Ⅱ型胶原蛋白对血清抗体和派氏集结细胞因子表达的影响

来源 :细胞与分子免疫学杂志 | 被引量 : 0次 | 上传用户:fisher58
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目的:探讨口服Ⅱ型胶原蛋白(CⅡ)对派[伊尔]氏集结(PP结)的形态学、细胞因子表达水平和血清特异性IgG、IgA、IgM含量的影响。方法:连续10 d给小鼠口服不同剂量的CⅡ,第11天和第21天用佐剂或CⅡ进行免疫,分别于第11天、第21天和第31天采集血液和PP结。PP结经HE染色后,镜下观察其增生的情况。用荧光实时定量RT-PCR法,检测PP结中IL-17、TNF-α、IFN-γ和TGF-β1 mRNA的水平。采用ELISA法检测血清抗CⅡIgG、IgA、IgM的水平。结果:口服CⅡ10 d后,PP结增生活跃,高剂量组可见清晰的帽状结构;血清中出现IgA,未见IgG和IgM水平增加;IL-17、TNF-α、IFN-γmRNA的表达受到抑制。以CⅡ初次免疫后,实验组IgA、IgM、IL-17的水平均低于对照组(P<0.05或P<0.01),TGF-β1的水平显著增加(P<0.05)。以CⅡ加强免疫后,高剂量组IgA的水平显著增加(P<0.05),实验组IgM的水平仍受到抑制(P<0.05或P<0.01),TGF-β1的水平高于对照组(P<0.05)。以佐剂免疫时PP结中细胞因子的表达与CⅡ免疫时相似,未见血清抗CⅡIgG、IgA、IgM水平的变化。结论:口服CⅡ能使血清中产生特异性IgA,抑制PP结IL-17、TNF-α、IFN-γ的基因表达,对CⅡ免疫后IgA、IgM的产生和IL-17 mRNA的表达具有一定的抑制作用。以上结果表明,血清特异性抗体的水平和细胞因子表达的变化在口服CⅡ诱导免疫耐受对类风湿性关节炎的治疗作用方面发挥着重要的作用。 Objective: To investigate the effects of oral C Ⅱ on the morphology, cytokine expression and serum specific IgG, IgA, IgM contents of pie [Il] buildup (PP). Methods: Mice were orally given different doses of CⅡ for 10 days. On the 11th and 21st days, mice were immunized with adjuvant or C Ⅱ. Blood and PP were collected on the 11th, 21st and 31st day respectively. PP knot HE stained, the microscope observed the proliferation of the situation. The levels of IL-17, TNF-α, IFN-γ and TGF-β1 mRNA in PP were detected by real-time quantitative RT-PCR. Serum anti-CⅡIgG, IgA and IgM levels were detected by ELISA. Results: After 10 days of oral CⅡ, the hyperplasia of PP knots was active and the cap-like structure was seen in the high-dose group. The level of IgA in serum was not seen and the levels of IgG and IgM were not increased. The expression of IL-17, TNF-α and IFN- . The levels of IgA, IgM and IL-17 in the experimental group were significantly lower than those in the control group (P <0.05 or P <0.01) after the initial immunization with CⅡ, and the levels of TGF-β1 were significantly increased (P <0.05). The level of IgA in the high-dose group was significantly increased (P <0.05), the level of IgM in the high-dose group was still inhibited (P <0.05 or P <0.01), and the level of TGF-β1 was higher than that in the control group 0.05). When immunized with adjuvant, the expression of cytokines in PP knots was similar to that of CⅡ immunization, but there was no change of serum anti-CⅡIgG, IgA and IgM levels. CONCLUSION: Oral administration of CⅡ can produce specific IgA in serum and inhibit the gene expression of PP-junctions IL-17, TNF-α and IFN-γ. The production of IgA and IgM and the expression of IL-17 mRNA after CⅡ immunization have certain Inhibition. The above results indicate that serum-specific antibody levels and changes in cytokine expression play an important role in the therapeutic effect of oral CII-induced immune tolerance on rheumatoid arthritis.
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